ObjectiveTo explore the relationship between acne vulgaris and gut microbiota. MethodsA total of 29 clinical cases diagnosed with moderate-to-severe acne vulgaris and 26 healthy individuals as control subjects were recruited. Fecal specimens were collected from all participants， and further analysis of gut microbial communities was performed by leveraging high-throughput sequencing techniques that target the hypervariable regions of 16S rRNA genes. ResultsAssociations between acne vulgaris and alterations in gut microbiota were identified. At the phylum level， the relative abundance of Bacteroidota exhibited a statistically significant elevation in the acne vulgaris cohort when compared with the healthy control group （P<0.01）， while Cyanobacteria was significantly lower in the acne group （P<0.01）. At the genus level， the top five different bacterial taxa in both groups were Bacteroides， Escherichia⁃Shigella， Klebsiella， Roseburia， and Parabacteroides. Among them， Bacteroides， Roseburia， and Parabacteroides were more abundant in acne patients. Linear discriminant analysis identified five biomarkers all belonging to the Bacteroidota phylum in the acne and control groups. These biomarkers belong to the phylum Bacteroidetes. ConclusionThere are significant differences in the composition of intestinal microbiota between acne patients and healthy people. Changes in the richness of specific bacterial genera may become new targets for the diagnosis and treatment of acne.

Receptor-interacting protein kinase 1 (RIPK1) plays an essential role in regulating the necroptosis and apoptosis in cerebral ischemia-reperfusion (I/R) injury. However, the regulation of RIPK1 kinase activity after cerebral I/R injury remains largely unknown. In this study, we found the downregulation of protein arginine methyltransferase 1 (PRMT1) was induced by cerebral I/R injury, which negatively correlated with the activation of RIPK1. Mechanistically, we proved that PRMT1 directly interacted with RIPK1 and catalyzed its asymmetric dimethylarginine, which then blocked RIPK1 homodimerization and suppressed its kinase activity. Moreover, pharmacological inhibition or genetic ablation of PRMT1 aggravated I/R injury by promoting RIPK1-mediated necroptosis and apoptosis, while PRMT1 overexpression protected against I/R injury by suppressing RIPK1 activation. Our findings revealed the molecular regulation of RIPK1 activation and demonstrated PRMT1 would be a potential therapeutic target for the treatment of ischemic stroke.

Objective:To study the optimal anastomotic angle of end-to-side anastomosis autogenous arteriovenous fistula (AVF).Methods:A case-report and case-series design was used to obtain clinical data on 10 patients with diabetic nephropathy from Department of Nephrology, the 905th Hospital of the Chinese People′s Liberation Army Navy from June 2024 to February 2025. The models of "radial artery-cephalic vein" end-to-side anastomosis in the forearm with anastomotic angles of 30°, 40°and 50°were established. Numerical simulation was used to analyze the blood flow in the model, and to study the effect of different anastomotic angles on blood flow. Wall shear stress (WSS), cross section flow velocity and flow rate, and relative residence time (RRT) were studied in the model. The Whitney test with Holm correction was used to evaluate the difference in the median RRT between the three angle models.Results:At the moment of 0.65 s, the area fraction of low wall shear stress (LWSS) in the 30° model was 7.7%, which was reduced by 2.4% and 3.7% compared to the 40°and 50°models, respectively. At the time of 0.2 s, the area proportions of high wall shear stress (HWSS) in the 30°, 40°and 50°models were 54.4%, 43.9% and 37.4%, respectively. At 0.2 s, the maximum cross section flow velocity reached 4.07, 3.84 and 3.67 m/s for the 30°, 40°and 50°models, respectively. In the cycle, the maximum mean flow velocity for the 30°model reached 1.20 m/s. The mean flow rates of the 30°, 40°and 50°models in the J-5 cross section were 349, 316, and 328 ml/min, respectivly. For patient 6, the area proportions of the RRT>1 region were 11.97%, 14.84% and 15.22% for the 30°, 40°and 50°models, respectively.Conclusions:The optimal anastomotic angle of "radial artery-cephalic vein" for end-to-side anastomosis AVF surgery in patients with diabetic nephropathy is 40°.

Objective To investigate the effect of miR-7975 on the malignant phenotype of oral squamous cell carcinoma(OSCC)and its potential mechanisms.Methods This study compared the expression levels of miR-7975 in different oral cell lines by qRT-PCR.miR-7975 mimic and miR-7975 inhibitor were transfected into OSCC cell lines HSC3 and HN4 respectively.Colony formation as-say,CCK8 assay,Transwell assay,and wound healing assay were conducted to evaluate the effects of miR-7975 on the malignant phe-notype of OSCC cells.Western blot was employed to analyze changes in the expression of EMT related proteins and proteins associated with the RAS/ERK signaling pathway.Subcutaneous tumor model of nude mice was used to further validate the tumorigenic effect of miR-7975 in vivo.Results The expression of miR-7975 was downregulated in OSCC cells.Overexpression of miR-7975 reduced the proliferation,migration,and invasion abilities of OSCC cells,whereas downregulation of miR-7975 enhanced these abilities.After miR-7975 overexpression,the expression of the EMT-related protein E-cadherin was upregulated,while N-cadherin,Vimentin,β-catenin,Snail,and Slug were downregulated.Additionally,the expression of proteins related to the RAS/ERK signaling pathway increased.Conversely,the expression of EMT and RAS/ERK signaling pathway-related proteins showed opposite changes when miR-7975 was downregulated.Compared to the control group,the volume and weight of tumors formed in nude mice were significantly smaller after miR-7975 overexpression,while they were significantly larger when miR-7975 expression was reduced.Conclusion miR-7975 exerts its tumor-suppressive effects by inhibiting the proliferation,migration,and invasion of OSCC through the regulation of EMT and the RAS/ERK signaling pathway.

Objective To investigate the value of CT radiomics for predicting effect of neoadjuvant chemotherapy(NACT)for locally advanced gastric cancer(LAGC).Methods Totally 325 LAGC patients who received NACT were retrospectively enrolled,among them 247 were taken as training set,while the rest 78 were taken as validation set.Tumor regression scale(TRG)was evaluated according to postoperation pathology after NACT,and the efficacy of NACT was evaluated.Univariate logistic regression was used to analyze and screen clinical predictors of effect of NACT,and clinical model was constructed.Radiomics features were extracted based on venous phase enhanced CT pre-and post-NACT,and Delta radiomics features(i.e.the ratio of the difference of pre-and post-NACT radiomics features and pre-NACT radiomics features)were calculated.The best features were screened based on pre-NACT,post-NACT and Delta radiomics features to construct radiomics labels,the optimal label was screened and used to construct combined model through combining clinical model.Receiver operating characteristic(ROC)curve was plotted,and the area under the curve(AUC)was calculated to evaluate predicting efficiency of the above models.Decision curve analysis(DCA)was performed to explore the clinical value of each model.Results In training set,significant effect was found in 67 cases,but not in 180 cases,while in validation set,significant effect was found in 18 cases but not in 60 cases.Borrmann classification of LAGC before NACT was the clinical predictor(P=0.031),and clinical model was constructed,which had AUC of 0.577 and 0.520 in training and validation sets,respectively.Based on pre-NACT,post-NACT and Delta radiomics features,19,14 and 17 best features were selected,and AUC of the established radiomics labels of Pre-Rad,Post-Rad and Delta-Rad in training set was 0.672,0.796 and 0.789,while in validation set was 0.558,0.805 and 0.666,respectively.Post-Rad was the optimal label,which was used to construct combined model.AUC of the obtained combined model in training and validation sets was 0.824 and 0.818,respectively,both higher than that of clinical model(both P＜0.001)but not different with that of Post-Rad(both P＞0.05).Taken 0.4 to 0.7 as the threshold,the combined model had higher clinical net benefit than the other two.Conclusion Venous CT radiomics could effectively predict effect of NACT for LAGC.Combining with clinical features could improve its predictive efficacy.

Objective To investigate the effect of miR-7975 on the malignant phenotype of oral squamous cell carcinoma(OSCC)and its potential mechanisms.Methods This study compared the expression levels of miR-7975 in different oral cell lines by qRT-PCR.miR-7975 mimic and miR-7975 inhibitor were transfected into OSCC cell lines HSC3 and HN4 respectively.Colony formation as-say,CCK8 assay,Transwell assay,and wound healing assay were conducted to evaluate the effects of miR-7975 on the malignant phe-notype of OSCC cells.Western blot was employed to analyze changes in the expression of EMT related proteins and proteins associated with the RAS/ERK signaling pathway.Subcutaneous tumor model of nude mice was used to further validate the tumorigenic effect of miR-7975 in vivo.Results The expression of miR-7975 was downregulated in OSCC cells.Overexpression of miR-7975 reduced the proliferation,migration,and invasion abilities of OSCC cells,whereas downregulation of miR-7975 enhanced these abilities.After miR-7975 overexpression,the expression of the EMT-related protein E-cadherin was upregulated,while N-cadherin,Vimentin,β-catenin,Snail,and Slug were downregulated.Additionally,the expression of proteins related to the RAS/ERK signaling pathway increased.Conversely,the expression of EMT and RAS/ERK signaling pathway-related proteins showed opposite changes when miR-7975 was downregulated.Compared to the control group,the volume and weight of tumors formed in nude mice were significantly smaller after miR-7975 overexpression,while they were significantly larger when miR-7975 expression was reduced.Conclusion miR-7975 exerts its tumor-suppressive effects by inhibiting the proliferation,migration,and invasion of OSCC through the regulation of EMT and the RAS/ERK signaling pathway.

Objective To investigate the value of CT radiomics for predicting effect of neoadjuvant chemotherapy(NACT)for locally advanced gastric cancer(LAGC).Methods Totally 325 LAGC patients who received NACT were retrospectively enrolled,among them 247 were taken as training set,while the rest 78 were taken as validation set.Tumor regression scale(TRG)was evaluated according to postoperation pathology after NACT,and the efficacy of NACT was evaluated.Univariate logistic regression was used to analyze and screen clinical predictors of effect of NACT,and clinical model was constructed.Radiomics features were extracted based on venous phase enhanced CT pre-and post-NACT,and Delta radiomics features(i.e.the ratio of the difference of pre-and post-NACT radiomics features and pre-NACT radiomics features)were calculated.The best features were screened based on pre-NACT,post-NACT and Delta radiomics features to construct radiomics labels,the optimal label was screened and used to construct combined model through combining clinical model.Receiver operating characteristic(ROC)curve was plotted,and the area under the curve(AUC)was calculated to evaluate predicting efficiency of the above models.Decision curve analysis(DCA)was performed to explore the clinical value of each model.Results In training set,significant effect was found in 67 cases,but not in 180 cases,while in validation set,significant effect was found in 18 cases but not in 60 cases.Borrmann classification of LAGC before NACT was the clinical predictor(P=0.031),and clinical model was constructed,which had AUC of 0.577 and 0.520 in training and validation sets,respectively.Based on pre-NACT,post-NACT and Delta radiomics features,19,14 and 17 best features were selected,and AUC of the established radiomics labels of Pre-Rad,Post-Rad and Delta-Rad in training set was 0.672,0.796 and 0.789,while in validation set was 0.558,0.805 and 0.666,respectively.Post-Rad was the optimal label,which was used to construct combined model.AUC of the obtained combined model in training and validation sets was 0.824 and 0.818,respectively,both higher than that of clinical model(both P＜0.001)but not different with that of Post-Rad(both P＞0.05).Taken 0.4 to 0.7 as the threshold,the combined model had higher clinical net benefit than the other two.Conclusion Venous CT radiomics could effectively predict effect of NACT for LAGC.Combining with clinical features could improve its predictive efficacy.

Objective To explore the effect of FBXW7 on ferroptosis in head and neck squamous cell carcinoma.Methods Head and neck squamous cell lines HN4 and HN6 were cultured in vitro.FBXW7 and SOX2 overexpression plasmids were constructed,and the plasmids were stably transfected into cell lines.The overexpression transfection efficiency was verified at the transcription level and protein level by qRT-PCR and Western blot experiments,respectively.The lipid peroxidation levels of head and neck squamous cell carcinoma cells with overexpressing FBXW7 were verified by measuring malondialdehyde(MDA),glutathione(GSH),and reactive ox-ygen species(ROS)levels.After treating cells with ferroptosis inhibitor Fer-1,the changes in cell viability were further detected to ver-ify the effect of FBXW7 on ferroptosis.The effect of transfection of the overexpressed plasmid on cellular pathways was detected by Western blot.Results HN4 and HN6 cell lines showed increased levels of lipid peroxidation after overexpression of FBXW7,and the ferroptosis inhibitor Fer-1 was able to effectively reverse the ferroptosis induced by overexpression of FBXW7.Western blot assay results showed that overexpression of FBXW7 reduced the expression of c-Myc,SOX2 and SLC7A11.Conclusion FBXW7 regulates the ex-pression of SOX2-SLC7A11 by degrading c-Myc,thereby effectively regulating ferroptosis in HNSCC.

Objective To explore the impact of knocking down Sec31A on the malignant phenotype of head and neck squamous cell carcinoma(HNSCC)and its possible mechanisms.Methods Transcriptome sequencing data of HNSCC tissues and adjacent tissues were obtained from the TCGA database,and the expression levels of Sec31A were compared.Immunohistochemical staining was used to analyze the expression of Sec31A in HNSCC tissues.Kaplan-Meier survival analysis was used to compare the relationship between Sec31A and the prognosis of HNSCC patients.Small interfering plasmids si-Sec31A and si-NC were transfected into HNSCC cell lines HN6 and HN4,and the impact of knocking down Sec31A on the biological behavior of HNSCC cells was detected through CCK-8 exper-iments,plate cloning experiments,scratch healing experiments,and Transwell experiments.Changes in the expression levels of PI3K/AKT/mTOR pathway related proteins in cells were detected after knocking down Sec31A with HN6 and HN4 through Western Blot(WB)experiments.Stable transfected cell lines of HN6 siSec31A and HN6 siNC were constructed and inoculated subcutaneously in nude mice to further verify the tumorigenic effect of Sec31A in vivo.Results TCGA data showed that Sec31A was higher in HNSCC tissues than in adjacent normal tissues(P＜0.01),and high expression of Sec31A was significantly correlated with poor prognosis in pa-tients(P＜0.05).Immunohistochemical staining showed that Sec31A was expressed stronger in HNSCC tissues than in normal tissues.In HN6 and HN4 cells,knocking down Sec31A resulted in significantly weaker proliferation,migration,and invasion abilities compared to the control group.Through WB experiments,it was found that transfection of si-Sec31A with HN6 and HN4 significantly reduced the expression levels of p-PI3K,p-AKT,and p-mTOR proteins.After knocking down Sec31A with HN6,the transplanted tumor volume in nude mice was significantly smaller than that in the control group.Conclusion Knocking down Sec31A can inhibit the proliferation,migration and invasion of HNSCC cells,possibly through the PI3K/AKT/mTOR pathway.